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Ganglion cell loss and vasculopathy observed in Mthfr+/- and Cbs (Montrer CBS Protéines)+/- mouse retinas may be milder than expected, not because of compensatory increases of enzymes in remethylation/transsulfuration pathways, but because downstream transsulfuration pathway products GSH, taurine, and H2S are maintained at robust levels.
In summary, high folate intake during pregnancy leads to pseudo-MTHFR deficiency, disturbed choline/methyl metabolism, embryonic growth delay and memory impairment in offspring. These findings highlight the unintended negative consequences of supplemental folic acid.
Study demonstrated that maternal MTHFR deficiency (i.e., in utero MTHFR deficiency) and early life exposure to vigabatrin separately and together alter the levels of proteins in the glutamatergic synapse
Mildly hyperhomocysteinemic Mthfr+/- mice demonstrate reduced ganglion cell function, thinner NFL (Montrer NEFL Protéines), and mild vasculopathy by 24 weeks.
DNA methylation (Montrer HELLS Protéines) patterns in undifferentiated spermatogonia are relatively stable in culture over time under conditions of altered methionine and MTHFR levels.
Data from Mthfr knockout mice (in homozygous/heterozygous matings) suggest that maternal genotype contributes to sensitivity to arsenic as embryotoxin (i.e., genetic predisposition to fetal resorption/congenital malformation in arsenic poisoning).
our results support an interaction between mild neonatal stress, the MTHFR genotype and sex
investigation of Mthfr regulation in an in vivo mouse model revealed temporal- and tissue-specific regulation that supports important roles for MTHFR in the developing embryo, and in postnatal brain and male reproductive tissues
A possible mechanism for the epigenetic involvement of Mthfr deficiency is proposed in the gender-dependent regulation of proteins associated with plasticity of the excitatory synapse.
These results showed that methylenetetrahydrofolate reductase deficiency impairs endothelial progenitor cell formation and increases endothelial progenitor cell senescence by endothelial nitric oxide synthase (Montrer NOS3 Protéines) uncoupling and downregulation of SIRT1 (Montrer SIRT1 Protéines).
Our findings indicate that the MTHFR gene polymorphism might play a role in the etiology of patients with recurrent miscarriage (RM) or repeated implantation failure (RIF). No adverse effects of different MTHFR haplotypes on embryo development were detected. Further studies on the biological role are needed to better understand the susceptibility to pregnancy complications
The meta-analysis suggested that the T allele of the rs1801133 polymorphism of MTHFR is a risk factor for coronary artery disease.
MTHFR C677T polymorphisms were significantly associated with recurrent pregnancy loss (RPL) in Bosnian women...
The 1298A>C polymorphism in the MTHFR gene is not a risk factor for ischemic stroke in pediatric patients. (Meta-analysis)
MTHFR SNPs are associated with bone turnover level in Chinese pregnant women. Homocysteine, osteocalcin (Montrer BGLAP Protéines) and lead contents in plasma are associated with the MTHFR gene A1298C polymorphism.
MTHFR 677 T may play a significant role in regard to the risk of preterm delivery, especially in the Asian population.
The MTHFR 677TT genotype is an independent risk factor for hyperhomocysteinemia in Tunisian rheumatoid arthritis patients.
Findings provide evidence for a relationship between two genes-three mutations-of the cardiovascular disease (CVD genes panel and recurrent pregnancy loss (RPL). These genotypes include MTHFR C677T homozygosity, MTHFR A1298C homozygosity, compound heterozygosity of the two MTHFR gene mutations.
Study indicated that MTHFR rs1801133, FGF5 (Montrer FGF5 Protéines) rs16998073 and CSK (Montrer CSK Protéines) rs1378942 were associated with increased the risk of obesity in the Chinese children.
Findings showed lower MTHFR mRNA expression in preeclampsia (PE) women. The MTHFR rs1537514C>G polymorphism was associated with lower PE risk and MTHFR mRNA expression. Lower expression of MTHFR mRNA was observed in women with hypermethylated promoter.
The protein encoded by this gene catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. Genetic variation in this gene influences susceptibility to occlusive vascular disease, neural tube defects, colon cancer and acute leukemia, and mutations in this gene are associated with methylenetetrahydrofolate reductase deficiency.
, 5,10-methylenetetrahydrofolate reductase (NADPH)
, methylenetetrahydrofolate reductase (NAD(P)H)
, methylenetetrahydrofolate reductase-like
, methylenetetrahydrofolate reductase